Peripheral Vascular Disease Flashcards
1
Q
There are how many types of blood vessels?
A
5
2
Q
What are the types of blood vessels?
A
Veins
Venules
Capillaries
Arteries
Arterioles
3
Q
Blood vessels that carry deoxygenated blood, Thin, less muscular wall
A
Veins/ venules
4
Q
Blood vessel with 3 less defined layers
A
Veins/ venules
5
Q
Blood vessels that distend more than arteries
A
Veins/ venules
6
Q
Blood vessels with valves to prevent backward flow
A
Veins/ venules
7
Q
75% total blood volume is in the
A
veins
8
Q
SNS can stimulate constriction of these blood vessels
A
veins
9
Q
These blood vessels use contraction of skeletal muscles to move blood flow
A
Veins/ venules
10
Q
Single layer blood vessels with thin walls that permits transport
A
Capillaries
11
Q
Blood vessels where oxygen and CO2 exchange
A
Capillaries
12
Q
Blood vessels that carry oxygen rich blood
A
Arteries/Arterioles
13
Q
Blood vessels with thick walls and three distinct layers
A
Arteries/Arterioles
14
Q
The inner layers of the arteries/ arterioles are
A
smooth
15
Q
The middle layer of the arteries/ arterioles
A
dilates/constricts
16
Q
The outer layer of the arteries/ arterioles
A
Anchor vessels
17
Q
Blood vessels where chemical, hormonal, neuronal factors effect constriction and dilation
A
Arteries/Arterioles
18
Q
The lymphatic system collects lymph from tissues and organs and transports into
A
venous circulation
19
Q
Permeable to large molecules ie: protein
A
lymph
20
Q
Muscular contraction of walls and tissue propels lymph towards
A
venous drainage
21
Q
Excess fluid from the arterial-venous filtration is absorbed by
A
lymphatic circulation
22
Q
Runs alongside the capillary bed
A
lymphatic system
23
Q
Hardening of arteries
A
Arteriosclerosis
24
Q
Plaque formation
A
Atherosclerosis
25
Injury to endothelium causes platelets and monocytes
to aggregate
26
Two types of lesions
Fatty streaks
fibrous plaques
27
Decreased flow of oxygen rich blood due to narrowed arterial lumen is caused by
Arteriosclerosis and atherosclerosis
28
Increased metabolic demands caused by arteriosclerosis and atherosclerosis leads to
ischemia
29
ischemia
an inadequate blood supply to an organ or part of the body causing pain
30
Smoking increases platelet aggregation leading to
clot formation
31
aggregation
clustering
32
Atherosclerosis clinical manifestations:
Coronary arteries
angina, MI
33
Atherosclerosis clinical manifestations:
Cerebral arteries
Stroke , TIA’s
34
Atherosclerosis clinical manifestations:
Aorta
aneurysm
35
Atherosclerosis of Extremities
Peripheral Artery Disease
36
Number 1 sign of Peripheral Artery Disease
Intermittent claudication
37
Pain caused by too little blood flow to muscles during exercise.
Claudication
38
What do the legs/feet look like with PAD?
Thin brittle shiny skin on legs/feet
Loss of hair on legs
Dependent rubor
Thickened toenails
39
What might you find while assessing legs/feet with PAD?
Diminished peripheral pulses
Prolonged capillary refill
40
Patients with advanced PAD will feel
Pain at rest
41
Patients with PAD may have what kind of ulcers?
dry, necrotic, delayed healing
42
Pain is distal to
diseased artery
43
Claudication may begin shortly after
activity begins
44
PAD:
Elevating legs makes pain _____ and foot becomes _____
worse and foot becomes pale
45
PAD:
Dangling (dependent) legs does what to pain? What color do the feet turn?
relieves pain – foot becomes deep red (rubor)
46
PAD:
Med that improves blood flow
Cilostazol
47
Onychomycosis is
A fungal infection of the nail
48
PAD diagnostic tests:
Sees blood flow in legs
Doppler study
49
PAD diagnostic tests:
Testing for claudication
Treadmill test
50
PAD diagnostic tests:
combines both ultrasound and Doppler procedures. The result is live, high-definition pictures of blood flow.
Duplex ultrasound
51
PAD diagnostic tests:
Non-invasive test performed by measuring the systolic blood pressure from both brachial arteries and from both the dorsalis pedis and posterior tibial arteries after the patient has been at rest in the supine position for 10 minutes
Arterial Brachial Index (ABI)
52
What patients need ABI?
Pt with diminished pulses
50 y or older with history of diabetes
53
Patients with an ABI <0.9 =
PAD
54
NORMAL ABI is
1 – 1.4
55
NORMAL ABI is because feet arterial BP
Is slightly higher than brachial
56
Cilostazol should enable pt to
walk longer periods of time without pain
57
Pt will aortoiliac disease –
assess femoral pulse
58
Carbon monoxide from tobacco binds to
hemoglobin depriving tissues of oxygen
59
Fluid exchange across capillary wall based on
hydrostatic and osmotic forces.
60
Hydrostatic pressure at arterial end is higher then
venous
61
Hydrostatic pressure at arterial end drives fluid into the
tissue space
62
At venous end of capillary, osmotic forces
reabsorb fluid back into capillary.
63
Any left over fluid goes into
lymphatic vessels
64
Interpretation of ABI:
> 1.30
Noncompressible
65
Interpretation of ABI:
0.41 - 0.90
Mid-Moderate PAD
66
Interpretation of ABI:
0.00 - 0.40
Severe PAD
67
PAD patient teaching
Promote exercise, dangle legs, do not elevated, no crossing legs, no heating pads
Weight reduction, smoking cessation, reduce BP
68
Platelet Inhibitors prevent
clots
69
Platelet Inhibitor med names
Aspirin
Clopidogrel (Plavix)
Cilostazol (Pletal)
70
Statins draw
cholesterol out of plaques
71
Endovascular Treatments
Balloon angioplasty, stent, atherectomy
72
After graft/stent, patient will likely be placed on
platelet inhibitor to keep stent/graft open
73
Surgery for partial and complete blockage
Bypass grafts
74
Autologous bypass graft
pt’s own vein
75
Dacron graft
Synthetic bypass graft
76
Nursing care post bypass
VS & Pulse check q15 min initially
Incision site – monitor for hematoma
Neurovascular checks (cap refill/temperature/color)
Edema expected, elevate EXT while in bed and ambulate as soon as possible
No leg crossing or prolonged dependent position
77
After fem-pop bypass – which pulse do you assess?
After fem-pop bypass, assess dorsalis pedis or tibial
78
Checking for complications:
Graft Occlusion
pallor, decreased pulses, cool skin temperature
79
Checking for complications:
Compartment Syndrome
Numbness, severe pain, edema, taunt skin
80
If there are complications after treatment surgery
Ambulate ASAP
81
Med given in recovery room
Plavix or may be kept on heparin drip
82
Stenosis and occlusions less frequent in
arms
83
Upper extremity arterial disease is usually the result of
atherosclerosis or trauma
84
S&S of Upper extremity arterial disease
Arm fatigue, pain with exercise, inability to hold objects
Cool, pales, decreased capillary refill
85
Diagnostic test to determine upper extremity arterial disease
Doppler studies
86
Artery providing blood flow to brain reverses to arm causing lightheadedness
Subclavian steal syndrome
87
Treatment for upper extremity arterial disease
PTA with stent or graft
88
PTA
Percutaneous Transluminal Angioplasty
89
Nursing after surgery for upper extremity arterial disease
Vascular checks – if no pulse – immediately contact physician
Keep arm at heart level or elevated after surgery
90
Aching/burning is ischemia, but a complete occlusion is
more severe pain, or complete loss of sensation
91
6 P’s
Pain
Pallor
Pulselessness
Paresthesia
Poikilothermia
Paralysis
92
Poikilothermia
the inability to regulate core body temperature
93
Parasthesia
Pins and needles
94
COLD / PALE FOOT – will turn
dusky
95
Balloon tipped catheter that removes embolus
Emergency embolectomy
96
If patient has adequate collateral circulation
Heparin or t-PA is given
97
t-PA :
tissue plasminogen activator (clot buster), an injection given right into clot
98
Arterial occlusions are diagnosed with
ultrasound and arteriogram
99
Nursing Management of arterial occlusion:
Prior to intervention:
BEDREST
Affected EXT level or slightly dependent
Keep EXT room temperature (no heating/cooling pads)
100
Nursing Management of arterial occlusion:
Med stopped 30 minutes prior to surgery
IV Heparin
101
Intermittent arteriolar vasoconstriction
Results in coldness/pallor/pain of fingertips, toes
Raynaud’s phenomenon
102
Reynaud's:
Rebound circulation causes
redness and pain
103
Skin color changes associated with Raynaud's
WHITE – then BLUE because of pooling of deoxygenated blood the RED from exaggerated blood flow during vasodilation
104
Raynaud’s phenomenon stimulus:
Cold, Stress, Nicotine
105
Raynaud’s phenomenon Treatment:
usually none required, possible Calcium Channel Blocker
106
idiopathic
no other condition (genetic)
107
Veins that lie just under the skin
Superficial Veins
108
Veins that run parallel to arteries
Deep Veins
109
Venous disorders cause
reduction in venous blood flow back up to heart
110
Result of Venous disorders
stasis of blood, edema, tissue breakdown (ulcers/cellulitis), increased susceptibility to cellulitis
111
Small vessels rupture from pressure, rbc’s escape into surrounding tissue
Hemosiderin
112
Chronic distension from increased pressure and incompetent valves
Chronic Venous insufficiency
113
Risk factors for Chronic Venous insufficiency:
Obesity, immobility, pregnancy, history of DVT
114
S&S of Chronic venous insufficiency:
edema, discolored skin – hemosiderin, draining wounds
115
Treatment for Chronic Venous insufficiency:
Elevate legs
Compression stockings
Monitor for complications (cellulitis/wounds)
116
S&S of Venous insufficiency
Varicose veins
Darkened, hard, leathery skin
Pain and heaviness
Restless leg syndrome
leg cramps or spasms (NOT intermittent claudication)
Itchy skin
Yellow toenails
117
Virchow Triad
1) Hypercoagulability
2) Stasis
3) Vascular injury
118
VTE
Venous thromboembolism
119
Hypercoagulability state
Clotting too much
120
Most common cause of this VTE factor:
Cancer malignancy
pregnancy and peri-partum (because of hormones)
Oestrogen therapy
Trauma or surgery of lower half of body
Hypercoagulability state
121
Venous wall gets nicked or damaged
Vascular wall injury
122
Most common cause of this VTE factor:
Trauma/injury
Venipuncture
Chemical irritation
Heart valve disease or replacement
Atherosclerosis
Indwelling catheters
Vascular wall injury
123
When blood is not moving
Circulatory stasis
124
Most common cause of this VTE factor:
Atrial fibrillation
Left ventricular dysfunction
Venous insufficiency or varicose veins
Venous obstruction from tumor
Obesity or pregnancy
Bedrest
Post op
Circulatory stasis
125
Aggregates of platelets within the vein, attached to wall
More common in lower EXT’s
Deep vein thrombosis
126
The 3 causes of deep vein thrombosis:
vein injury (phlebitis from IV/chemo),
stasis
hypercoagulability
127
Clinical Manifestations of deep vein thrombosis:
Unilateral swelling of effected leg
Deep vein: edema, swelling, warmth, tenderness, red, concern of PE
Superficial veins: similar, usually dissolve spontaneously
Homan’s sign
128
Treatments for deep vein thrombosis
Anticoagulant therapy (monitor labs to direct)
elevate legs - pillow under legs not knee
compression stocking
Thrombectomy – mechanical clot removal with balloon stent
129
Once anticoagulation therapy started –
ambulate as soon as possible
130
Diagnosing DVT
Blood work (coagulation studies),D dimer, duplex ultrasound
131
Obstruction of pulmonary artery or one of its branches by a thrombus that originated in VENOUS system OR right side of heart
Pulmonary embolism (PE)
132
Symptoms of PE depend on
size of thrombus and area of pulmonary artery occluded
133
Symptoms of PE:
DYSPNEA
Chest pain, anxiety, tachycardia, dry cough
134
Diagnosing PE :
CT Angiogram or V/Q SCAN
135
Medical management of a stable patient with PE:
Lovenox/heparin
136
Medical management of an unstable patient with PE:
Thrombolytic therapy
Embolectomy – Interventional radiology
137
PE is not a ventilation problem, it is a
Perfusion problem
138
Most dangerous form of PE
Saddle PE
139
Nursing care of patient with PE
Monitoring thrombolytic therapy
Bleeding precautions
Manage Pain
Manage oxygen therapy
Relieve anxiety
Education : Patient will be discharged on long term anticoagulation
IVC filter placement (in groin) before discharge
140
IVC (inferior vena cava) filter does what? For how long?
Catches clots. Left in for one year
141
Platelet inhibitors & Anticoagulants does what to clots?
slow, stop, prevent clot. DOES NOT BREAK
142
Names of platelet inhibitors :
acetylsalicylic acid (Aspirin)
clopidogrel (Plavix)
cilostazol (Pletal)
143
Anticoagulant PO med that blocks liver’s use of vit K to produce clotting factors. Takes up to 72 hours to work
No precise antidote, but can give VIT K
Warfarin (Coumadin)
144
Newer PO anticoagulant meds:
no specific blood tests to monitor
No specific antidote exists
Can not stop taking suddenly
Dabigatran (Pradaxa)
Rivaroxaban (Xarelto)
Apixaban (ELIQUIS) PO only
145
INR
International Normalized Ratio
146
Foods that should be reduced/ eaten in moderation while taking warfarin (coumadin)
Green, leafy vegs
147
Give more coumadin when INR is
below 2
148
Give less coumadin when INR is
above 3
149
Normal INR is
between 2-3
150
Injectable anticoagulants that act rapidly to block formation of thrombin from prothrombin
Enoxaparin (Lovenox) (SQ)
Heparin (IV or SQ prophylactic)
151
Rate of heparin determined protocol –
aPTT lab values should be higher that normal with heparin(1.5 – 2.5 times normal Aptt = 60-80)
152
Will continue use of Heparin while starting Warfarin until
INR is 2
153
Antidote to Heparin :
protamine sulfate
154
Lovenox can be used for DVT, post operative, what type of surgery?
ortho surgery
155
All patients on heparin:
Bleeding precautions
all stool is tested for blood (guaiac)
CBC is usually daily – not every 3 days
156
HIT
Heparin induced thrombocytopenia
157
Low platelet count due to heparin
HIT - Heparin induced thrombocytopenia
158
Abnormally dilated, tortuous veins
Incompetent valves
Varicose veins
159
Clinical Manifestations of varicose veins:
Asymptomatic if superficial
Deep veins – dull ache, cramps heaviness, fatigue, swelling
160
Nonsurgical treatments for varicose veins:
Thermal Ablation, sclerotherapy, laser
161
Surgical treatments for varicose veins:
Ligation and stripping – vein is pulled out with the metal wire
162
Compression therapy is mostly done with what type of ulcer?
venous ulcers
163
Mechanical debridement –
wet-to-dry dressings
164
Autolytic debridement –
application of dressings that allow lysozymes in wound exudate to naturally breakdown nonviable tissue – Aquacel
165
Autolytic debridement med
Aquacel
166
Aquacel holds a lot of
drainage
167
Chemical debridement med
Santyl (collagenase)
168
Ulcer treatments
Antiseptic agents
Antibiotics
Debridement
hyperbaric oxygenation
wound vac
169
What kind of diet is appropriate for a patient with leg ulcers?
High protein diet rich in vitamins
170
Condition where the Microbes enter skin via entry point,
Toxins released into subcutaneous tissues, causing Swelling, redness, warmth and pain
Cellulitis
